Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024141 (systemic lupus erythematosus)
 44,322 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Since the beginning of the pandemia caused by the Human Immunodeficiency Virus several reports have described cases of infection by HIV1 in patients bearing rheumatic diseases. The infection by HIV 1 in patients with Systemic Lupus Erythematosus (SLE) and Chronic Cutaneous Lupus Erythematosus (CCLE), however, seems to be elusive. As far as we know, only 3 cases of HIV infection associated with SLE have been published. Furthermore, we have not been able to find out any report concerning HIV infection in patients bearing CCLE. The aim of the present article is to present a case of a female patient with CCLE that subsequently developed an infection with human immunodeficiency virus.
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PMID:Chronic cutaneous lupus erythematosus and subsequent infection with HIV1. 130 64

Thirty four sera from: 12 patients with Systemic Lupus Erythematosus (SLE), 9 with Subacute Cutaneous Lupus Erythematosus (SCLE) and 13 with Discoid Lupus Erythematosus (DLE) (disseminatus 3, localised 10) were tested for the presence of: (a) anti-thyroglobulin and anti-microsomal autoantibodies (b) anti-Sm/RNP, anti-doublestranded. DNA (anti-ds. DNA), anti-single-Stranded. DNA (anti-ss. DNA), anti-cardiolipin (anti-Cl), anti-SSA, anti-SSB, Antinuclear Antibodies (ANA). T3, T4, TSH levels were also determined. Five patients with SLE (41.6%), 4 with SCLE (44.4%), and 2 with DLE (15.3%) had thyroid autoantibodies and only three of the 41 controls (7.3%). Five patients (14.7%), especially from SLE and SCLE groups, had biochemical hypothyroidism whereas only one had hyperthyroidism. Statistical evaluation for the possible coexistence of thyroid autoantibodies with a panel of lupus characteristic autoantibodies, revealed highly significant correlations with anti-Sm/RNP, IgG (p = 0.003) and anti-ds. DNA, IgM (p = 0.012). It may be concluded, that not only SLE but also SCLE predisposes to autoimmune thyroid disease and the prevalence of the latter is related to a great extent to the subset of the LE spectrum. From these results and from the inhibition experiments, it seems that some of the specific mono- or polyclonal autoantibodies may be multiple organ reactive.
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PMID:Thyroid autoantibodies in the subsets of lupus erythematosus: correlation with other autoantibodies and thyroid function. 750 37

Cutaneous lupus erythematosus may be related to maternal autoantibody production in the neonatal lupus syndrome, or may occur later in childhood, with or without findings of systemic lupus erythematosus (SLE). In the first section, we will discuss the transient, passively transferred neonatal disease, and in the second, we will discuss the persistent, actively acquired forms of lupus erythematosus in childhood.
Lupus 1997
PMID:Cutaneous lupus erythematosus during the neonatal and childhood periods. 906 61

We developed and validated a measurement instrument (CLASI-Cutaneous Lupus Erythematosus Disease Area and Severity Index) for lupus erythematosus that could be used in clinical trials. The instrument has separate scores for damage and activity. A group of seven American Dermato-Rheumatologists and the "American College of Rheumatology Response Criteria Committee on SLE (systemic lupus erythematosus)" assessed content validity. After a preliminary session, we conducted standardized interviews with the raters and made slight changes to the instrument. The final instrument was evaluated by five dermatologists and six residents who scored nine patients to estimate inter- and intra-rater reliability in two sessions. Consultation with experts has established content validity of the instrument. Reliability studies demonstrated an intra-class correlation coefficient (ICC) for inter-rater reliability of 0.86 for the activity score (95% confidence interval (CI) = 0.73-0.99) and of 0.92 for the damage score (95% CI = 0.85-1.00). The Spearman's rho (Sp) for intra-rater reliability for the activity score was 0.96 (95% CI = 0.89 to 1.00) and for the damage score Sp was 0.99 (95% CI = 0.97-1.00). Clinical responsiveness needs to be evaluated in a prospective clinical trial, which is ongoing.
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PMID:The CLASI (Cutaneous Lupus Erythematosus Disease Area and Severity Index): an outcome instrument for cutaneous lupus erythematosus. 1629 85

Cutaneous lupus erythematosus can be induced or precipitated by a variety of drugs. Among the cutaneous variants of lupus, subacute cutaneous lupus erythematosus is the one most often associated with drug intake. The time lag between drug intake and skin eruption makes the clinical association less obvious, and the condition is often overlooked. We report on a 50-year-old woman with previously diagnosed systemic lupus erythematosus who had a severe cutaneous flare-up seven weeks after starting treatment with terbinafine for suspected onychomycosis.
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PMID:[Cutaneous lupus erythematosus induced by terbinafine]. 1721 73

Skin involvement is a frequent presenting manifestation of systemic lupus erythematosus (SLE). Cutaneous lupus erythematosus (CLE), frequently occurring without SLE, may be even more common than SLE. Until recently, clinical instruments to measure skin involvement in CLE did not exist, hampering clinical research in this field. In this paper the present authors describe outcome instruments for SLE and outline the considerations underlying the design and validation of an outcome instrument for CLE, the cutaneous lupus disease area and severity index. These studies serve as a model for development and validation of standardized instruments that can be applied to other cutaneous diseases, particularly autoimmune diseases, in order to facilitate epidemiologic studies and clinical trials.
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PMID:Development of the CLASI as an outcome instrument for cutaneous lupus erythematosus. 1753 37

Cutaneous lupus erythematosus (LE; syn LE-specific skin disease) is an autoimmune disease with well-defined skin manifestations often accentuated in a photodistribution and frequently associated with specific autoantibodies. These clinical observations have led to numerous laboratory studies related to the role of ultraviolet light, as well as studies of the cascade of immunologic events involved in the pathogenesis of cutaneous LE. We discuss the epidemiologic, clinical, and laboratory findings of cutaneous LE, including the classification of disease subsets. We review the evidence for abnormal photoreactivity in LE with an overview of the cellular, molecular, and genetic factors that may underlie this abnormality. As there is yet no convincing animal model of cutaneous LE, many studies remain descriptive in nature. To arrive at an understanding of the potential mechanisms underlying the development of cutaneous lupus, we discuss the role of ultraviolet light-mediated induction of apoptosis, antigen presentation, genetic factors, and mediators of inflammation. In addition, we consider the role and importance of humoral and cellular factors, synthesizing the current understanding of the pathophysiology of cutaneous lupus.
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PMID:Pathophysiology of cutaneous lupus erythematosus. 1809 49

Cutaneous lupus erythematosus (CLE) is a heterogeneous disorder with a wide range of skin manifestations. In the second part of this review, diagnostic procedures and treatment options in CLE are summarized.The diagnosis of the various subtypes of CLE is based on patients's history,clinical findings,laboratory features, and histological and immunofluorescent examinations of skin biopsies. In case of systemic organ involvement, further adequate technical investigations are necessary. The therapy has to be adjusted to the subtype of CLE and its inflammatory activity as well as the extent of skin involvement. The skin manifestations of CLE are primarily treated by topical therapy, such as glucocorticosteroids, in combination with antimalarials. The response of CLE to immunosuppressive drugs that control organ involvement in systemic lupus erythematosus is often disappointing. Recent advances in biotechnology resulted in the development of several novel systemic agents for the treatment of autoimmune diseases; however, controlled clinical trials are still necessary for the approval of new therapies in CLE.
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PMID:Diagnostic approach and treatment of cutaneous lupus erythematosus. 1819 Apr 33

Cutaneous lupus erythematosus (LE) may present in a variety of clinical forms. Three recognized subtypes of cutaneous LE are acute cutaneous LE (ACLE), subacute cutaneous LE (SCLE), and chronic cutaneous LE (CCLE). ACLE may be localized (most often as a malar or 'butterfly' rash) or generalized. Multisystem involvement as a component of systemic LE (SLE) is common, with prominent musculoskeletal symptoms. SCLE is highly photosensitive, with predominant distribution on the upper back, shoulders, neck, and anterior chest. SCLE is frequently associated with positive anti-Ro antibodies and may be induced by a variety of medications. Classic discoid LE is the most common form of CCLE, with indurated scaly plaques on the scalp, face, and ears, with characteristic scarring and pigmentary change. Less common forms of CCLE include hyperkeratotic LE, lupus tumidus, lupus profundus, and chilblain lupus. Common cutaneous disease associated with, but not specific for, LE includes vasculitis, livedo reticularis, alopecia, digital manifestations such as periungual telangiectasia and Raynaud phenomenon, photosensitivity, and bullous lesions. The clinical presentation of each of these forms, their diagnosis, and the inter-relationships between cutaneous LE and SLE are discussed. Common systemic findings in SLE are reviewed, as are diagnostic strategies, including histopathology, immunopathology, serology, and other laboratory findings. Treatments for cutaneous LE initially include preventive (e.g. photoprotective) strategies and topical therapies (corticosteroids and topical calcineurin inhibitors). For skin disease not controlled with these interventions, oral antimalarial agents (most commonly hydroxychloroquine) are often beneficial. Additional systemic therapies may be subdivided into conventional treatments (including corticosteroids, methotrexate, thalidomide, retinoids, dapsone, and azathioprine) and newer immunomodulatory therapies (including efalizumab, anti-tumor necrosis factor agents, intravenous immunoglobulin, and rituximab). We review evidence for the use of these medications in the treatment of cutaneous LE.
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PMID:Cutaneous lupus erythematosus: issues in diagnosis and treatment. 1982 38

Cutaneous lupus erythematosus includes a variety of lupus erythematosus specific skin lesions that, in some cases, can be disfiguring and refractory to conventional therapy. This short report describes our experience in treating six patients with severe, refractory subacute cutaneous lupus erythematosus with monthly cyclophosphamide pulses, followed by azathioprine as maintenance therapy. Significant clinical improvement of the subacute cutaneous lupus erythematosus lesions was achieved in all patients, with four patients in complete remission and two in partial remission. Mean time to clinical response was 4.33 +/- 1.36 months. Minor adverse events and no relapses were noted in a follow-up period of more than 3 years.
Lupus 2010 May
PMID:Pulse cyclophosphamide treatment for severe refractory cutaneous lupus erythematosus. 2017 72


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